Presented By – Dr. Shivesh Mishra

July 29th , 2014

Department of Periodontics

I.T.S. Dental College, Hospital & Research CenterGreater Noida

Moderator- Dr. Shivjot ChhinaPerceptor-Dr. Saurav Kumar

Introduction to Aging General Effects of aging Effect of aging on peridontiumo Gingival epitheliumo Gingival connective tissueo Periodontal ligamento Cementumo Alveolar Boneo Bacterial plaqueo Immune response

Systemic diseases & Periodontal health Conclusion

The process of becoming older, a process that is genetically determined and environmentally modulated.1

It includes the complex interaction of biologic, psychologic, and sociologic process over time.

Thus, in contrast to the chronological milestones which mark life stages in the developed world, old age in many developing countries is seen to begin at the point when active contribution is no longer possible." (Gorman, 2000)

The geriatric population has been growing fast over the last decades all over the world, changing demographics.

Changes in biochemical and physiological processes occur with aging in all body tissues, including the peridontium.

Human ageing induces histophysiological and clinical alterations in oral tissues.2

These alterations must be understood to differentiate pathological conditions from the altered physiology of oral tissues resulting from ageing .3

External

Hair Brittle, Less Abundant, Gray

Skin Dehydration, Decreased Elasticity, Thermo Sensitive

Eyes Diminished Vision, Enopthalmos

Nose Diminished Sense Of Smell

SecretoryGlands

Diminished Epithelial Activity

Internal

Renal Decreased renal blood flow Leading to waterretention, Difficulty in removing waste products

Vascular Rise in systolic blood pressure

GIT Constipation and gas accumulation due tohypotonic musculature

Gonads Decrease estrogen and androgen secretion

Liver Decrease hepatic function

Pancreas Decrease function (diabetes)

Alternations in oral motor functions

Lip posture Drooling, angular cheilosis

Muscles of mastication

Efficiency of Mastication decreases

Tongue Speech, dysphagia, traumatic bite injury

Swallowing Dysphagia

Taste Loss of sensation or decreased sensation

The tissues that support the teeth are called the periodontium, which consists of gingiva, periodontal ligament, cementum, and alveolar bone.

Anatomical and functional changes in periodontal tissues have been reported as being associated with the ageing process.4

Thining of epithelium & diminished keratinization.5

Increased epithelial permeability to pathogens

Decreased resistance to functional trauma.

Conflicting results have been reported regarding the shape of the retepegs.

A flattening of retepegs and an increase in the height of the epithelial ridges associated with ageing were both demonstrated.

Gingival sample obtained from a 25-year-old healthy subject. Normal aspect of epithelium layers, dermal papillae and connective tissue, without signs of proliferation (HE staining, ×10).

Gingival sample obtained from a 66-year-old subject. Thickening of epithelium due to acanthosis (HE staining, ×10).

Rom J Morphol Embryol 2013, 54(3 Suppl):811–815

In a morphological 3-dimensional study of the epithelium-connective tissue interface, connective tissue ridges were observed to be more prevalent in young individuals whereas connective tissue papillae were predominant in old individuals.

The change from ridges to papillae involves the formation of epithelial cross-ridges with advanced age.4

Number of cellular elements decreases as age increases.

The fibroblasts are the main cells in the synthesis of periodontal connective tissue.

In vivo and in vitro studies have shown functional and structural alterations in fibroblasts associated with ageing.6-8

Gingival fibroblasts (GF) may be constantly affected by oral bacteria and their products, such as the lipopolysaccharides(LPS), present in their cell walls.

The LPS induces GF to release some inflammatory cytokines such as prostaglandin E2 (PGE2), interleukin (IL)-1, and plasminogen activator (PA) 6, 14.

The influence of these inflammatory mediators on both GF and periodontal ligament fibroblasts (PLF) might account for the severity of periodontal disease.6

The effect of aging on location of junctional epithelium has been the subject of much speculation.

The apical migration of the junctional epithelium, with consequent gingival recession, has been discussed.

Although such a migration is associated with aging, the loss of insertion caused by aging alone may not seem to have clinical significance.9

Gingival recession progression may occur due to several factors, such as passive eruption caused by physiological wear of teeth, a consequence of anatomically thin tissues and toothbrushing trauma.

Apparently, gingival recession is not an avoidable physiological process caused by aging, but a cumulative and progressive effect from periodontal disease or trauma over time.5

Carranza’s clinical periodontology 10th edition Chapter -6 ,Page No. 94

Coarser and denser gingival connective tissue

Qualitative and quantitative changes to collagen

include;

◊ increased rate of conversion of soluble to insoluble

collagen.

◊ increased mechanical strength

◊ increased denaturing temperature

These results indicate increased collagen stabilization

caused by the changes in the macromolecular

conformation

There is also a reduction in the organic matrix production and in vascularization, and an increase in the number of elastic fibers.

Decreased number of fibroblasts

Decreased organic matrix production

Decreased epithelial cell rests

Decreased number of collagen fibers

↓

reduction or loss in tissue elasticity

Cells of PDL have reduced mitotic activity

Thickness of the periodontal ligament varies and may reduce due to the reduction in the force applied by masticatory muscles along the time in subjects with complete dentition or having dental elements with no antagonist.10

On the other hand, when several elements are missing, there might be an overload on the existing remaining teeth, with consequent periodontal ligament thickening.11

Increase in cemental width is a common finding.

Increase may be 5 to 10 times with increasing age.12

Increase in width is greater apically and lingually.13

Deposition takes place mainly in apical region to compensate for the physiological wear of teeth.

Reduction of bone mass.

More irregular periodontal surface of bone.

Less regular insertion of collagen fibers.

Increased bone resorption.

The reduction in bone formation might be due to a decrease in osteoblast-proliferating precursors or to decreased synthesis and secretion of essential bone matrix proteins.6

The extracellular matrix surrounding osteoblasts has been shown to play an important role in bone metabolism.

A possible dysfunction of this matrix might occur concomitantly with the ageing process.14

Oxygen-free radicals have been reported to cause cellular damage and, consequently, contribute to the ageing process.15,16

In an in vitro study, oxygen radical-treated fibronectin (FN) was found to inhibit bone nodule formation by osteoblastswhen compared to intact FN.

This finding suggested that intact FN plays an important role in osteoblast activity .

FN damaged by oxygen radicals during the ageing process might be related to less bone formation

Although age is a risk factor for the reduction of the bone mass in osteoporosis,it is not causative and therefore distinguished from physiologic aging process.

Age has been recognized as having much less effect in altering the host response

Difference between younger and older individuals can be demonstrated for T and B cells, cytokines,andnatural killer cells,but not polymorphonuclear cells and macrophages activity.

McArthur 17 concludes that “measurement of indicators of immune & inflammatory competency suggested that ,within the parametes tested ,there was no evidence for age related changes in host defences correlating with periodontitis in an elederly group of individuals ,with and without disease.”

NUTRIENT INCREASED

FUNCTION

DECREASED FUNCTION

VITAMIN A Bacterial adhesion

Salivary Antimicrobial

Properities,immunoglobulin And

Lymphocytes Production

VITAMIN E ----------------

--------------

Antibody Synthesis,response Of

Lymphocytes,phagocytic Action

VITAMIN C

----------------

--------------

Phagocytic Action Of Neutrophils

And Macrophages,antibody

Response

ZINC

----------------

---------------

Antibody Response,phagocytic

Function Of Macrophages

RIBOFLAVIN,VIT

B6,PANTHOTENIC ACID

--------------------

------------

Antibody

synthesis,cytotxic T-

cell toxicity,

lymphocyte response

FOLIC ACID AND

VITAMIN B 12

--------------------

------------

Cytotoxic T cell

toxicity,lymphocyte

production,phagocytic

function of neutrophils

IRON

--------------------

------------

Lymphocytic

proliferation,neutrophil

cytotoxic

activity,antibody

response

Loss of tooth substance – Attrition

Degree of attrition is influenced by

◦ Musculature

◦ Consistency of food

◦ Tooth hardness

◦ Occupational factors

◦ Habits like bruxism

◦ Continuous tooth eruption

Gingival recession

Dentogingival plaque accumulation increases with

increase in age:

• with Increase in hard tissue surface area resulting from

gingival recession

• The surface characteristics of the exposed root

surfaceas a substrate for plaque formation

For sub gingival plaque ,increased number of entric

rods and pseudomonads in older adults.

Periodontal pathogens specifically including an

increased role for P. gingivalis and decreased role for A. actinomycetemcomitans

Infectious diseases, such as periodontitis, cause inflammation and contribute to levels of overall infection and inflammation in the body and may trigger the beginning and/or the progression of other diseases such as diabetes and arteriosclerosis.18

There are two mechanisms through which infection and inflammation apparently located in periodontal pockets may harm general health:19

The passage of periodontal pathogens and their products into circulation (bacteremia)

The passage of locally produced inflammatory

mediators into circulation

JADA 2006;137(10 supplement):26S-31S.

It is suggested that the potential interactions between diabetes and periodontitis seem to enhance the morbidity of these two diseases.20

The chronic hyperglycemic condition of diabetes is associated with damage, dysfunction, or failure of various organs and tissues, including the periodontium.

It is due to the increased risk for infections in patients with diabetes, impairment of the synthesis of collagen and glycosaminoglycans by gingival fibroblasts, and increased crevicular fluid collagenolytic activity, Altered wound healing.21

It has been demonstrated by a meta-analysis study that patients with types 1 and 2 diabetes had worse oral hygiene and higher severity of gingival and periodontal diseases, compared to nondiabetic subjects.22

A multivariate risk analysis showed that subjects with type 2 diabetes had approximately threefold increased odds of having periodontitis compared with subjects without diabetes, after adjusting for confounding variables including age, sex and oral hygiene measures.23

Periodontal and cardiovascular diseases are common inflammatory conditions in the human population, atherosclerosis being the major component of the latter.

Loesche et al did a study on association between periodontal disease and coronary heart disease.

They found that in patients with periodntal diseases there are 1.84 times more CHD

Subgingival plaque flora

Increased access to flora (compared to supra gingival plaque)

Via ulcerated epithelial lining of the pocket

Underlying connective tissue

Antimicrobial potential in

tissues

Cellular debris

Systemic circulation

Alterations in serum components of clotting mechanisms

Elevated levels of fibrinogen

Risk of future coronary heart disease

Destroyed

A meta-analysis study indicated that individuals with periodontitis had 1.14 times higher risk of developing coronary heart disease.24

The more severe the periodontal disease the easier the periodontal pathogens could enter the circulation, reaching blood vessels and atherosclerotic lesions.

Another linkage between periodontal disease and CHD is the level of C-reactive protein, which is an acute-phase reactant in response to infection or trauma and its high sustained level was associated with advanced periodontitis.25

Ridker et al. demonstrated that C-reactive protein levels predict the risk of coronary events.26

Goal of periodontal treatment is to preserve function and prevent the progression of inflammatory disease

- Factors must be considered in treatment planningPatients

- Medical and health status - Medications - Life style behaviors- Ability to perform oral hygiene procedures - Ability to tolerate treatment - Amount of remaining periodontal support, tooth type

Operator side

- Decrease the length of surgical time - Maintain open communication - Minimize trauma- Recalculate medication dosages- Schedule morning appointment

- Non surgical approach – first treatment of choice

- Surgical approach – depends on nature and extent of disease

- Palliative supportive periodontal care – patients who are not

comply with treatment, have poor oral hygiene, medically or

mentally compromised, functionally impaired.

XEROSTOMIA

Fluoride rinses and dentifrices

Reduced consumption of alcohol, tobacco, spicy and acidicfoods

Frequent water in take

Artificial salivary substitutes

Burning mouth

Salivary substitutes

Diphenhydramine, koalin, lidocaine mouth wash

Aging dental patients have particular oral and general health conditions that dentists should be familiar with detecting, consulting, and treating.

Medical diseases and conditions that occur more often with age may require modification to periodontal preventive tools as well as the planning and treatment phases of periodontal care.

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